According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.

Although the group of people at risk for SAH is younger than the population usually affected by stroke, the risk still increases with age. Young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. The risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. Risk of SAH is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels.

Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. However, lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked. Some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. There is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic SAH, though confirmation of this association is hindered by a lack of studies. Approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with SAH are bending over or lifting heavy objects at the onset of their symptoms.

Overall, about 1 percent of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture.

SAH is often associated with a poor outcome. The death rate (mortality) for SAH is between 40 and 50 percent, but trends for survival are improving. Of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever. Delay in diagnosis of minor SAH (mistaking the sudden headache for migraine) contributes to poor outcome. Factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age. Factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma, or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission.

So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries a better prognosis than SAH with aneurysm; however, it is still associated with a risk of ischemia, rebleeding, and hydrocephalus. Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.

The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. It is difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. People with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as those who do not. They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit. However, more than 90 percent of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12 have a good outcome.

There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seems to increase risk for delayed ischemia and a worse outcome. The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of poor outcome.

Prognosis is also very poor when IVH results from intracerebral hemorrhage related to high blood pressure and is even worse when hydrocephalus follows. It can result in dangerous increases in ICP and can cause potentially fatal brain herniation. Even independently, IVH can cause morbidity and mortality. First, intraventricular blood can lead to a clot in the CSF conduits blocking its flow and leading to obstructive hydrocephalus which may quickly result in increased intracranial pressure and death. Second, the breakdown products from the blood clot may generate an inflammatory response that damages the arachnoid granulations, inhibiting the regular reabsorption of CSF and resulting in permanent communicating hydrocephalus.

Brain contusions and subarachnoid hemorrhages are commonly associated with IVH. The bleeding can involve the anterior communicating artery or the posterior communicating artery.

In both adults and infants, IVH can cause dangerous increases in ICP, damage to the brain tissue, and hydrocephalus.

Intracranial hemorrhage is a serious medical emergency because the buildup of blood within the skull can lead to increases in intracranial pressure, which can crush delicate brain tissue or limit its blood supply. Severe increases in intracranial pressure (ICP) can cause brain herniation, in which parts of the brain are squeezed past structures in the skull.

Intracranial bleeding occurs when a blood vessel within the skull is ruptured or leaks. It can result from physical trauma (as occurs in head injury) or nontraumatic causes (as occurs in hemorrhagic stroke) such as a ruptured aneurysm. Anticoagulant therapy, as well as disorders with blood clotting can heighten the risk that an intracranial hemorrhage will occur.

Some evidence suggests that magnesium sulfate administered to mothers prior to early preterm birth reduces the risk of cerebral palsy in surviving neonates. Due to the risk of adverse effects treatments may have, it is unlikely that treatments to prevent neonatal strokes or other hypoxic events would be given routinely to pregnant women without evidence that their fetus was at extreme risk or has already suffered an injury or stroke. This approach might be more acceptable if the pharmacologic agents were endogenously occurring substances (those that occur naturally in an organism), such as creatine or melatonin, with no adverse side-effects.

Because of the period of high neuronal plasticity in the months after birth, it may be possible to improve the neuronal environment immediately after birth in neonates considered to be at risk of neonatal stroke. This may be done by enhancing the growth of axons and dendrites, synaptogenesis and myelination of axons with systemic injections of neurotrophins or growth factors which can cross the blood–brain barrier.

Of the infants that survive, there may be as many as 1 million a year that develop cerebral palsy, learning difficulties or other disabilities. Cerebral palsy is the most common physical disability in childhood, and it is characterized by a lack of control of movement. Other neurological defects that can occur after a neonatal stroke include hemiparesis and hemi-sensory impairments Some studies suggest that when tested as toddlers and preschoolers, children who previously had neonatal strokes fall within normal ranges of cognitive development. Less is known about longer-term cognitive outcome, but there has been evidence that cognitive deficits may emerge later in childhood when more complex cognitive processes are expected to develop.

In 2004 the first adequately large scale study on the natural history and long-term prognosis of this condition was reported; this showed that at 16 months follow-up 57.1% of patients had full recovery, 29.5%/2.9%/2.2% had respectively minor/moderate/severe symptoms or impairments, and 8.3% had died. Severe impairment or death were more likely in those aged over 37 years, male, affected by coma, mental status disorder, intracerebral hemorrhage, thrombosis of the deep cerebral venous system, central nervous system infection and cancer. A subsequent systematic review of nineteen studies in 2006 showed that mortality is about 5.6% during hospitalisation and 9.4% in total, while of the survivors 88% make a total or near-total recovery. After several months, two thirds of the cases has resolution ("recanalisation") of the clot. The rate of recurrence was low (2.8%).

In children with CVST the risk of death is high. Poor outcome is more likely if a child with CVST develops seizures or has evidence of venous infarction on imaging.

Cerebral venous sinus thrombosis is more common in particular situations. 85% of patients have at least one of these risk factors:

- Thrombophilia, a tendency to develop blood clots due to abnormalities in coagulation, e.g. factor V Leiden, deficiency of protein C, protein S or antithrombin, or related problems

- Nephrotic syndrome, a kidney problem causing protein loss in the urine

- Chronic inflammatory diseases, such as inflammatory bowel disease, lupus and Behçet's disease

- Pregnancy and puerperium (the period after giving birth)

- Particular blood disorders, especially polycythemia vera and paroxysmal nocturnal hemoglobinuria

- Use of estrogen-containing forms of hormonal contraception

- Meningitis and infections of the ear, nose and throat area such as mastoiditis and sinusitis

- Direct injury to the venous sinuses

- Medical procedures in the head and neck area

- Sickle cell anemia

- Dehydration, primarily in infants and children

- Homocystinuria

A 1994 community-based study indicated that two out of every 100,000 people suffered from SCSFLS, while a 2004 emergency room-based study indicated five per 100,000. SCSFLS generally affects the young and middle aged; the average age for onset is 42.3 years, but onset can range from ages 22 to 61. In an 11-year study women were found to be twice as likely to be affected as men.

Studies have shown that SCSFLS runs in families and it is suspected that genetic similarity in families includes weakness in the dura mater, which leads to SCSFLS. Large scale population-based studies have not yet been conducted. While a majority of SCSFLS cases continue to be undiagnosed or misdiagnosed, an actual increase in occurrence is unlikely.

IIAs are uncommon, accounting for 2.6% to 6% of all intracranial aneurysms in autopsy studies.

Mortality of IIA is high, unruptured IIA are associated with a mortality reaching 30%, while ruptured IIA has a mortality of up to 80%. IIAs caused by fungal infections have a worse prognosis than those caused by bacterial infection.

Intracranial aneurysms may result from diseases acquired during life, or from genetic conditions. Lifestyle diseases including hypertension, smoking, excessive alcoholism, and obesity are associated with the development of brain aneurysms. Cocaine use has also been associated with the development of intracranial aneurysms.

Other acquired associations with intracranial aneurysms include head trauma and infections.

Several complications can occur as a result of SCSFLS including decreased cranial pressure, brain herniation, infection, blood pressure problems, transient paralysis, and coma. The primary and most serious complication of SCSFLS is spontaneous intracranial hypotension, where pressure in the brain is severely decreased. This complication leads to the hallmark symptom of severe orthostatic headaches.

People with cranial CSF leaks, the rarer form, have a 10% risk of developing meningitis per year. If cranial leaks last more than seven days, the chances of developing meningitis are significantly higher. Spinal CSF leaks cannot result in meningitis due to the sterile conditions of the leak site. When a CSF leak occurs at the temporal bone surgery becomes necessary in order to prevent infection and repair the leak. Orthostatic hypotension is another complication that occurs due to autonomic dysfunction when blood pressure drops significantly. The autonomic dysfunction is caused by compression of the brainstem, which controls breathing and circulation.

Low CSF volume can cause the cerebellar tonsil position to descend, which can be mistaken for Chiari malformation; however when the CSF leak is repaired the tonsil position often returns to normal (as seen in upright MRI) in this "pseudo-Chiari" condition.

A further, albeit rare, complication of CSF leak is transient quadriplegia due to a sudden and significant loss of CSF. This loss results in hindbrain herniation and causes major compression of the upper cervical spinal cord. The quadriplegia dissipates once the patient lies supine. An extremely rare complication of SCSFLS is third nerve palsy, where the ability to move one's eyes becomes difficult and interrupted due to compression of the third cranial nerve.

There are documented cases of reversible frontotemporal dementia and coma. Coma due to a CSF leak has been successfully treated by using blood patches and/or fibrin glue and placing the patient in the Trendelenburg position. Empty sella syndrome, a boney structure that surround the pituitary gland, occurs in CSF leak patients.

It is not known what percentage of people with IIH will remit spontaneously, and what percentage will develop chronic disease.

IIH does not normally affect life expectancy. The major complications from IIH arise from untreated or treatment-resistant papilledema. In various case series, the long-term risk of ones vision being significantly affected by IIH is reported to lie anywhere between 10 and 25%.

The prevalence of intracranial aneurysm is about 1-5% (10 million to 12 million persons in the United States) and the incidence is 1 per 10,000 persons per year in the United States (approximately 27,000), with 30- to 60-year-olds being the age group most affected. Intracranial aneurysms occur more in women, by a ratio of 3 to 2, and are rarely seen in pediatric populations.

On average, IIH occurs in about one per 100,000 people, and can occur in children and adults. The median age at diagnosis is 30. IIH occurs predominantly in women, especially in the ages 20 to 45, who are four to eight times more likely than men to be affected. Overweight and obesity strongly predispose a person to IIH: women who are more than ten percent over their ideal body weight are thirteen times more likely to develop IIH, and this figure goes up to nineteen times in women who are more than twenty percent over their ideal body weight. In men this relationship also exists, but the increase is only five-fold in those over 20 percent above their ideal body weight.

Despite several reports of IIH in families, there is no known genetic cause for IIH. People from all ethnicities may develop IIH. In children, there is no difference in incidence between males and females.

From national hospital admission databases it appears that the need for neurosurgical intervention for IIH has increased markedly over the period between 1988 and 2002. This has been attributed at least in part to the rising prevalence of obesity, although some of this increase may be explained by the increased popularity of shunting over optic nerve sheath fenestration.

It may cause seizures but cephalohematoma and caput will not cause seizure

The majority (90%) result from applying a vacuum to the head at delivery (Ventouse assisted delivery). The vacuum assist ruptures the emissary veins (connections between dural sinus and scalp veins) leading to accumulation of blood under the aponeurosis of the scalp muscle and superficial to the periosteum. Subgaleal hematoma has a high frequency of occurrence of associated head trauma (40%), such as intracranial hemorrhage or skull fracture. The occurrence of these features does not correlate significantly with the severity of subgaleal hemorrhage.

Death occurs in about 10% of cases and people do well about 70% of the time. This is a large improvement from the 1960s due to improved ability to image the head, better neurosurgery and better antibiotics.

Cerebral vasospasm is the prolonged, intense vasoconstriction of the larger conducting arteries in the subarachnoid space which is initially surrounded by a clot.

Significant narrowing develops gradually over the first few days after the aneurysmal rupture. This spasm usually is maximal in about a week's time following haemorrhage.

Vasospasm is the one of the leading causes of death after the aneurysmal rupture along with the effect of the initial haemorrhage and later bleeding.

Obligatory hibernators such as the ground squirrels show resistance to ischemia/reperfusion (I/R) injury in liver, heart, and small intestine during the hibernation season when there is a switch from carbohydrate metabolism to lipid metabolism for cellular energy supply. This metabolic switch limits anaerobic metabolism and the formation of lactate, a herald of poor prognosis and multi-organ failure (MOF) after I/R injury. In addition, the increase in lipid metabolism generates ketone bodies and activates peroxisome proliferating-activated receptors (PPARs), both of which have been shown to be protective against I/R injury.

Causes of increased foetal-maternal haemorrhage are seen as a result of trauma, placental abruption or may be spontaneous with no cause found.

Up to 30 mL of foetal-maternal transfusion may take place with no significant signs or symptoms seen in either mother or foetus. Loss in excess of this may result in significant morbidity and mortality to the fetus. Foetal-maternal haemorrhage is one cause of intrauterine death (IUD).

Fungi and parasites may also cause the disease. Fungi and parasites are especially associated with immunocompromised patients. Other causes include: "Nocardia asteroides", "Mycobacterium", Fungi (e.g. "Aspergillus", "Candida", "Cryptococcus", "Mucorales", "Coccidioides", "Histoplasma capsulatum", "Blastomyces dermatitidis", "Bipolaris", "Exophiala dermatitidis", "Curvularia pallescens", "Ochroconis gallopava", "Ramichloridium mackenziei", "Pseudallescheria boydii"), Protozoa (e.g. "Toxoplasma gondii", "Entamoeba histolytica", "Trypanosoma cruzi", "Schistosoma", "Paragonimus"), and Helminths (e.g. "Taenia solium"). Organisms that are most frequently associated with brain abscess in patients with AIDS are poliovirus, "Toxoplasma gondii", and "Cryptococcus neoformans", though in infection with the latter organism, symptoms of meningitis generally predominate.

These organisms are associated with certain predisposing conditions:

- Sinus and dental infections—Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. "Prevotella", "Porphyromonas", "Bacteroides"), "Fusobacterium", "S. aureus", and Enterobacteriaceae

- Penetrating trauma—"S. aureus", aerobic streptococci, Enterobacteriaceae, and "Clostridium" spp.

- Pulmonary infections—Aerobic and anaerobic streptococci, anaerobic gram-negative bacilli (e.g. "Prevotella", "Porphyromonas", "Bacteroides"), "Fusobacterium", "Actinomyces", and "Nocardia"

- Congenital heart disease—Aerobic and microaerophilic streptococci, and "S. aureus"

- HIV infection—"T. gondii", "Mycobacterium", "Nocardia", "Cryptococcus", and "Listeria monocytogenes"

- Transplantation—"Aspergillus", "Candida", "Cryptococcus", "Mucorales", "Nocardia", and "T. gondii"

- Neutropenia—Aerobic gram-negative bacilli, "Aspergillus", "Candida", and "Mucorales"